Asbestos-induced chemiluminescence response of human polymorphonuclear leukocytes

Our plain-English summary of Asbestos-induced chemiluminescence response of human polymorphonuclear leukocytes, by M. Rola-Pleszczynski, D. Rivest, M. Bérardi (Environmental Research, 1984).

The study

• Authors: M. Rola-Pleszczynski, D. Rivest, M. Bérardi
• Journal: Environmental Research
• Published: 1984;33(1):1-6
• Cited by: 26 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Products of the oxidative metabolism of polymorphonuclear leukocytes (PMN), namely hydrogen peroxide and superoxide, may play a role in tissue injury at sites of inflammation. Oxidant production by PMN was measured by the luminol-enhanced chemiluminescence (CL) of cells exposed in vitro to asbestos fibers. Human peripheral blood PMN were incubated with 1-1000 micrograms/ml of UICC chrysotile B asbestos fibers opsonized with either normal or heat-inactivated human serum. CL was measured over 210 min and revealed a peak response at 45 min; this response was delayed in comparison to control CL induced by Staphylococcus aureus (5-10 min) and represented approximately 50% of that of the latter. Although maximal CL was generated by asbestos concentrations of 100-500 micrograms/ml, significant CL was observed at concentrations as low as 0.5-1 micrograms/ml. Opsonization of asbestos fibers with heat-inactivated serum markedly depressed CL responses, suggesting that complement activation by asbestos fibers may be important in the generation of CL by PMN. In view of the previously reported accumulation of PMN in the lungs of asbestos-exposed animals, this study suggests that oxidant production by PMN may mediate some of the pathological effects of asbestos fibers.

In plain English

This laboratory experiment tested how human white blood cells called polymorphonuclear leukocytes (PMN) respond to asbestos fibers outside the body. PMN from normal human blood were mixed with UICC B chrysotile asbestos fibers that had first been coated with human serum. The researchers measured the light the cells gave off (chemiluminescence), which reflects their production of reactive oxygen chemicals. The response rose with dose. Significant responses occurred at 0.5 to 500 micrograms per milliliter, with the maximum at 100 to 500. Above 800 the response fell. After 1 hour, cell death reached about 50% at 500 and 80% at 1000 micrograms per milliliter. Compared with Staphylococcus aureus bacteria, asbestos caused a slower response that peaked at about 45 minutes. Its peak values were about 50% as high, but the area under the curve was the same. Heat-inactivating the serum before coating the fibers almost completely abolished the response. The authors attributed this to heat-sensitive serum components, presumably complement. They suggested that oxidants made by these cells in exposed lungs may cause some of the lung changes from prolonged asbestos exposure.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: in vitro laboratory experiment on human blood cells
• Who was studied: Polymorphonuclear leukocytes (PMN) isolated from normal human venous blood; number of donors not stated; laboratory at the Université de Sherbrooke, Quebec, Canada
• Exposure: Standard UICC B (Canadian) chrysotile asbestos fibers, incubated with 10% human serum before use (opsonized), at a range of concentrations in micrograms per milliliter; compared with serum-coated Staphylococcus aureus bacteria
• Main results:
  • Asbestos produced significant chemiluminescence responses in PMN at concentrations of 0.5 to 500 micrograms per milliliter
  • Maximum chemiluminescence was at 100 to 500 micrograms per milliliter; above 800 micrograms per milliliter the response became progressively lower
  • No significant PMN death after 1 hour at up to 150 micrograms per milliliter; death reached about 50% at 500 and 80% at 1000 micrograms per milliliter
  • The asbestos-induced response peaked at about 45 minutes, versus 5 to 10 minutes for S. aureus
  • Peak asbestos-induced chemiluminescence reached 50% of that for S. aureus
  • The areas under the curve for asbestos- and S. aureus-induced chemiluminescence were the same; the authors judged total oxidative metabolism probably similar
  • When serum was heat-inactivated before coating the asbestos fibers or the bacteria, chemiluminescence was almost completely abolished
  • The authors interpreted the response as dependent on heat-labile serum components, presumably complement
• The authors' conclusion: The authors suggested that some lung changes from prolonged asbestos exposure may be caused by highly reactive oxidants generated by asbestos fibers in PMN attracted into the exposed lungs
• Limitations the authors state:
  • At high asbestos concentrations, the dose-response results reflect both oxidant production and the killing of the cells producing it

Topics

Medical terms in this study, explained in our Lexicon: Superoxide, Inflammation, UICC, Chrysotile.

Related studies

• Cellular mechanisms of reactive oxygen metabolite generation from human polymorphonuclear leukocytes induced by crocidolite asbestos — T. Ishizaki, E. Yano, et al. (1997)
• Crocidolite-induced reactive oxygen metabolites generation from human polymorphonuclear leukocytes — T. Ishizaki, E. Yano, et al. (1994)
• Production of reactive oxygen metabolites induced by asbestos fibres in human polymorphonuclear leucocytes — M. Hedenborg, M. Klockars (1987)
• The chemiluminescent response of human phagocytic cells to mineral dusts — I.P. Gormley, M.J. Kowolik, et al. (1985)
• Chemiluminescent detection of induced reactive oxygen metabolite production of human polymorphonuclear leucocytes by anthophyllite asbestos — T. Iwata, N. Kohyama, et al. (2002)
• The involvement of ionic interactions during asbestos-induced enzyme release from polymorphonuclear leukocytes — J.G. Elferink, M. Deierkauf, et al. (1989)

Browse more research in Environmental Research, or return to medical research.